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Life Protection > Morphology and Biology of Viruses > Flashcards

Morphology and Biology of Viruses Flashcards

1
Q

describe the main criteria for virus classification

A
  • Type and organisation of genome: DNA/RNA, single or double stranded, genome relatedness
  • Viral replication strategy: eg does it go through reverse transcription?
  • Structure and size of the virion: envelope, most viruses also icosahedral
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2
Q

Describe further criteria for viral classification

A

Host range
Tissue tropism
Pathogenicity
Mode of transmission
Physiochemical properties
Antigenic properties of the virion

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3
Q

Describe HIV

A

Envelope
Viral gp120 & gp41
2 copies of RNA
Reverse transcriptase
Integrase
Protease

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4
Q

Describe the hep viruses and the current vaccines for them

A

A: Enteric transmission
B, C, D: Non enteric transmission, persistent
E: Non enveloped, Icosahedral, single stranded + sense RNA
There are vaccines for Hep A and B
There is a Hep E vaccine used in china
Hep B vaccine is also used for hep D
Currently hay trials for therapeutic + prophylactic hep C vaccines

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5
Q

Describe Hep A in detail

A

Most common viral hepatitis
Picornaviridae family
Naked (no envelope), icosahedral
Single stranded RNA
+ve sense
Incubation (days): 15-45, mean 25
Onset: Acute, mainly infects children, young adults
Transmission: Foecal-oral
Sexual: possible but less likely

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6
Q

Describe Hep B in detail

A

Hepadnaviridae family, enveloped, 42nm
Icosahedral nucleocapsid
Circular DNA partially double stranded
Complete virus and incomplete particles
Tubular filaments & spherical particles composed of envelope proteins – hep B surface antigen
Incubation (days): 30-150, mean 75
Onset: Insidious or acute
Age preference: Young adults, babies, toddlers
Transmission: Faecal-oral, Percutaneous, Perinatal, Sexual
Can cause chronic and acute infection
Most people can fully recover in a few months.

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7
Q

Using percentages good clinical and epidemiological features of hepatitis B

A
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8
Q

Describe hepatitis D

A

Single stranded, negative sense, circular RNA
Viral envelope is made of HBAg
The virus requires Hep B virus to be present in the cell for its replication.
Infection can occur simultaneously or after hep B infection.
Transmission: contact with blood or other body fluids. Mother to child transmission at birth can also occur.

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9
Q

Describe hepatitis C

A

Flaviviridae family, enveloped, icosahedral
Single stranded RNA
NS1 non structural protein 1
E proteins are major envelope proteins of the virus
Incubation (days): 15-120, mean 50
Onset: Insidious, more common in adults
Transmission: Fecal-oral, though can also be Percutaneous, Perinatal, Sexual (though less likely)

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10
Q

Describe norovirus

A
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11
Q

Describe Rotavirus

A

GI infection: vomiting, diarrhea, abdo pain, fever
Most common in infants and young children
Once exposed symptoms take approx 2 days
No antivirals, but vaccines available – live oral vaccine

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12
Q

Describe the structure of rotavirus

A
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13
Q

What are the viral proteins for rotavirus and how does it replicate?

A

Structural proteins: VP1-VP7. Non structural: NSP1-NSP6
Infects and replicates in intestinal epithelial cells
Outmost layer has VP7 and VP4
These are important in virus attachment and entry

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14
Q

Describe the replication cycle for rotavirus.

A

Virus binds to receptors and enters cell by endocytosis
Virus loses its outer layer
Within virus structure dsRNA can replicate
This is because virus has a protein VP6 that acts as a channel and allows movement of RNA
Inside virus core there are VP1, VP2 and VP3
These are involved in transcription
Viral proteins are made in infected cell cytoplasm
Core assembly of single and double shelled particles in cytoplasm

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15
Q

Describe measles symptoms

A

Very contagious, spread by droplet infection
Fever, cough, runny nose, red eyes, sore throat
2 days later small white (Koplik’s) spots may appear in the mouth.
3-5 days after symptoms start: rash on face and spreads to neck, trunk, arms, legs, and feet.
When the rash appears, a person’s fever may spike
After a few days, the fever subsides and the rash fades.

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16
Q

Describe the structure of measles virus

A

Enveloped
RNA single stranded
Negative sense
Paramyxoviridae family
Pleomorphic (meaning occurs in many forms)
100-300nm

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17
Q

Describe mumps

A
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18
Q

Describe the structure of the mumps virus

A

Paramyxovirus
pleomorphic
enveloped
helical nucleocapsid
ss RNA linear genome

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19
Q

Describe Rubella

A

Togavirus family, enveloped
single stranded RNA, icosahedral
An acute viral disease causes fever and rash
mild disease in children and young adults
Rash/fever for 2-3 days
Spread by coughing and sneezing

20
Q

Describe Rubella

A

Togavirus family, enveloped
single stranded RNA, icosahedral
An acute viral disease causes fever and rash
mild disease in children and young adults
Rash/fever for 2-3 days
Spread by coughing and sneezing

21
Q

What is congenital rubella?

A

Birth defects if acquired by a pregnant woman, esp early pregnancy:
Deafness
Cataracts
heart, liver and spleen defects
Damage to foetal brain

22
Q

Describe adenoviruses

A

Different serotypes exist, most cause resp illness
May also cause gastroenteritis, conjunctivitis, cystitis, rash.
No envelope, icosahedral
DNA double stranded, linear

23
Q

Describe papillomavirus

A

No envelope, icosahedral
Circular, double stranded DNA
Papovaviridae family
Different serotypes
Some cause infections in the genital tract or cervical cancer

24
Q

Describe the structure of parovirus

A

Non-enveloped, single stranded DNA
small 22nm
Nucleocapsid icosohedral
Incubation period between 10-21 days
The virus has a receptor which allows it to attach to erythrocyte progenitor cells
Parvovirus B19 inhibits erythropoesis
Shortened life span of RBCs <120 days, viraemia present (virus in blood)

25
Q

Describe the clinical manifestations of parovirus

A

“slapped-cheek” rash, red rash on trunk and limbs.
May have a low-grade fever, malaise a few days before the rash breaks out. Rash may itch.
Resolves in 7-10 days
Gloves and socks syndrome
Arthropathy
Transient aplastic crisis
Chronic red cell aplasia
Neutropenia, thrombocytopenia and pancytopenia

26
Q

How is paro virus transmitted?

A

Respiratory route
mother to the foetus transmission - this is more of a concern in the first trimester and if the mother does not have IgG antibodies against the virus
No specific drug to treat Parvovirus B19 infection.

27
Q

Describe influenza

A

Airborne virus producing feverish illness
Causes serious illness in immunocompromised
Orthomixoviridae (family)
lipid envelope derived from host cell membrane.

28
Q

Label and describe this influenza structure

A

These are embedded in the lipid bilayer of the viral envelope.
Matrix protein 2, M2= ion channel protein
The ribonucleoprotein complex comprises viral RNA segments associated with the viral proteins.
The matrix (M1) protein is associated with both ribonucleoprotein and the envelope.

29
Q

Describe the influenza subtypes

A

Type A - Most serious, affects mammals and birds
Genetic cross-over between strains can lead to pandemic
Subtyped according to its surface Ags- (HA) and (NA)
Type B: affects humans, minor outbreaks
C: affects humans, endemic, similar to common cold

30
Q

Describe the replication cycle of influenza

A

Uses haemagglutinin to attach to sialic acid, enters by endocytosis
Virus envelope fuses w endosome, triggering uncoating
Viral nucleocapsid released into cytoplasm
Copies of viral RNA and mRNA made, mRNA translated in cytoplasm
Early viral proteins required for replication/transcription are transported back to the nucleus.
Late in infection cycle, M1 and NS2 proteins facilitate nuclear export of newly made viral ribo nuclear proteins.
RNA segments assembled within nucleocapsid and bud at plasma membrane

31
Q

How does the influenza virus mutate?

A

Surface Ags of Influenza A mutate rapidly bc:
Viral RNA polymerase involved in replication has low selectivity and no proof reading mechanism
Therefore mutants are generated and spread rapidly.
Two patterns of mutation: antigenic drift and antigenic shift

32
Q

Describe antigenic drift associated with influenza

A

Continual viral mutation
Mutations are often minor with no effect on function
Changes accumulate to create new “drifted strains”
Drifted strains produce illness
Some strains co-exist
Occurs in around 2 to 8 years

33
Q

Describe antigenic shift associated with influenza

A

Type A only
Genetic reassortment: mixing genetic material between strains, when they infect the same host
Creates novel strains ppl dont have immunity to.
Rapid spread - pandemic
Mixed strains from diff species= mas virulent/fuera control

34
Q

What is the current strategy in dealing with the different strains of influenza?

A

Global Influenza Network estimate the strain of virus before the following season and recommend vaccines
Limitations: errors in the estimate
manufacturing difficulties
time constraints, lack of resources
antigenic drift continues (vaccine mismatch)

35
Q

Explain how HIV infects and replicates inside a host cell.

A

HIV Gp120 protein binds to CD4. CCR5 T co receptor binds Gp120, enabling HIV to enter the T helper cell.
Reverse transcriptase copies viral RNA-> double stranded proviral DNA, which then undergoes ps.

Virus envelope proteins are also translated, transported in the G.app.Virus envelope proteins incorporate onto cell membrane.
Virus particle buds from the host cell, becoming wrapped in the cell membrane, producing a new viral envelope.

36
Q

What are the options for a primary viral infection?

A

Replication at the site of entry
Remain at the site of entry
Examples: Influenza, Rhino virus
Replicate at site of entry then spread, eg VZ virus

37
Q

Describe secondary infections

A

Infection with a 2nd organism, eg Candida albicans (thrush) if patient given antibiotics that have removed the protective flora
2* infections can also happen following an infection eg HIV that compromises immunity
Bacterial pneumonia can also happen after viral respiratory tract infections in a healthy individual.

38
Q

Outline the types of viral entry

A

Faecal oral route: Norovirus, Rotavirus
Blood: HIV, Hepatitis B and C
Body fluids: Epstein Barr virus
Resp tract: Influenza, Rhinovirus, VZ virus
Skin cuts: Papilloma, Mol.contagiousum (Poxvirus)
Sexual: Papilloma, Herpes simplex virus, HIV
Animal/insect bites: Lassa fever

39
Q

Which viruses cause acute and which viruses cause chronic disease?

A

Acute: Rabies, Rhinovirus, Influenza, Rotavirus
Chronic: Hep B and C, but in some cases infection can be cleared

40
Q

How can prenatal viruses be more pathogenic?

A

Vertical transmission: Foetus unable to mount immune response. Mode of entry also via placenta
eg rubella can be transmitted–> congenital rubella
Parvovirus infection in pregnancy – most of us have Abs to Parvovirus B19. Infection can show slapped cheek appearance – during early stages of pregnancy risk of hydrops fetalis.

41
Q

Describe the ways in which viruses can avoid detection by the immune system

A

Latency: After primary infection, enter sites eg dorsal root ganglia, remain latent.
Don’t replicate fully, evade detection.

Replicate in privileged sites: HIV. Cytomegalovirus: downregs MHC I, hinders Ag presentation

Release decoy particles: diverts response, eg Hep B

42
Q

Describe Papillomavirus

A

Non-enveloped
Circular double stranded DNA
More than 100 HPV types identified
High risk: HPV 16, 18, 31, 45
Linked to development of cervical carcinoma and other malignancies

43
Q

How does HPV infect our cells

A

Virus infects epithelial cells, which have dif layers and differentiate
As cells leave basal layer and move up they stop dividing- If cell is not replicative virus may struggle to replicate
So, virus infects basal layers, migrates to cell nucleus
Genome established, replication can occur

44
Q

Describe the cancer-causing mechanism with HPV

A

HPV encodes early genes(E2,6,7) + late genes(L1,2)
E6 interferes w P53 tumour suppressor protein
E7 interferes w retinoblastoma tumour suppressor
E2 inhibits E6 and E7 (cancer causing) expression
As HPV integrates into host genome, E2 viral gene splits
E2 ya no functions, E6 and 7 expression not inhibited
Uncontrolled E6/E7 oncoproteins=epithelial cells cannot leave the cell cycle

E6 also activates the telomerase gene
Cancer cells make telomerase which keeps telomere intact.
Cells do not age and continue to divide

45
Q

Describe Zika

A

Flaviviridae family
Enveloped, single strand +sense RNA
Small – 50nm
Transmitted by mosquitoes
Number of infants born with microcephaly high in areas where Zika virus was first reported- first trimester at greatest risk.

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